Mycoplasma Pneumoniae Pneumonia

Mycoplasma Pneumoniae Pneumonia

Pathology and Pathogenesis

Mycoplasmas are the smallest (0.2–0.8 μm) free-living bacteria, but they lack a true cell wall. They are facultative anaerobes, except for Mycoplasma pneumoniae, the most common pulmonary pathogen, which is a strict aerobe. Although it is primarily an infection of young adults, it can attack the elderly. The most common clinical syndrome is tracheobronchitis, with one-third of patients developing a mild but persistent pneumonia. Mycoplasma pneumonia is rarely biopsied, because positive cold agglutinin and specific complement fixation antigen assays establish the diagnosis. Biopsied cases show lymphocytic or neutrophilic bronchiolitis with alveolar wall inflammation and fibrinous exudates [17].

Symptoms and Signs

Mycoplasma pneumoniae pneumonia closely resembles typical pneumonia in the clinical manifestations, such as fever,

cough, and purulent sputum. However, patients with Mycoplasma pneumoniae pneumonia commonly have upper respiratory tract manifestations (otitis, bullous myringitis, and mild nonexudative pharyngitis). Extrapulmonary features, such as unexplained watery diarrhea, thrombocytosis, and hemolysis, are also common.

CT Findings

Common thin-section CT (TSCT) findings include centrilobular small nodules and branching linear opacity lesions (tree- in-bud pattern) in a patchy distribution, bronchial wall thickening, and areas of ground-glass opacity (GGO) and consolidation in a lobular or segmental distribution [18, 19] (Fig. 18.4). The abnormalities tend to have a patchy unilateral or asymmetric bilateral distribution, but may be diffuse. Another common abnormality is thickening of the peribronchial interstitium. The CT findings of Mycoplasma pneumonia in children include lobar or segmental consolidation with pleural effusion and regional lymphadenopathy and mild volume loss similar to those of bacterial lobar pneumonia [19]. Most patients with Mycoplasma pneumonia recover

Fig. 18.3 Lymphangitic metastasis along bronchovascular bundles manifesting as vascular tree-in-bud sign in a 59-year-old man who has pancreas head cancer. (a–c) Lung window images of serial CT scans obtained at same level over the follow-up period of 6 months show evolving lung lesion from tree-in-bud sign (arrows in a and b) to localized area of lobular

consolidation or a poorly defined nodule (arrow in c) in the right lower lobe. (d) High-magnification photomicrograph of surgical lung biopsy obtained from right lower lobe and at similar time to (c) discloses tumor cells (arrows) tracking arteriolar walls (definition-wise, lymphangitic tumor spread). Please note patent arteriolar lumen without cancer cells

completely; however, a small percentage, particularly children, develops bronchiectasis and bronchiolitis obliterans [20].

concomitant inflammatory reaction into the parenchyma adjacent to the airways [17].

Centrilobular small nodules and branching linear opacity lesions on TSCT reflect the presence of cellular inflammatory bronchiolitis. Lobular or segmental consolidation is related to pneumonia caused by extension of infection and

Treatment response is good if timely diagnosed and treated with effective antibiotics, but severe adult respiratory distress syndrome and macrolide-resistant Mycoplasma pneumonia have been reported [21].

Fig. 18.4 Mycoplasma pneumoniae pneumonia in a 2-year-old man. (a, b) Lung window images of CT scans (2.5-mm section thickness) obtained at levels of cardiac ventricle (a) and suprahepatic inferior vena

cava (b), respectively, show extensive ground-glass opacity in both lungs. Also note poorly formed centrilobular small nodules (arrowheads) and tree-in-bud signs (arrows) in both lungs

Fig. 18.5 Mycobacterium intracellulare pulmonary disease in a 53-year-old woman. (a, b) Lung window images of consecutive CT scans (2.5-mm section thickness) obtained at level of inferior pulmonary veins show tree-in-bud signs (arrows) in both lungs. Also note bronchiectasis with (open arrows) or without mucus plugging especially in right middle lobe and lingular division of left upper lobe. (c) Low-magnification

photomicrograph (×40) of pathologic specimen obtained from a different patient with nontuberculous mycobacterial pulmonary disease exhibits bronchiolocentric (membranous bronchiole, arrows) chronic inflammation, fibrosis, and granuloma formation. (d) High-magnification photomicrograph (×100) discloses granulomas (arrows) with surrounding chronic inflammation and fibrosis along membranous bronchioles

Fig. 18.6 Diffuse panbronchiolitis in a 38-year-old man. (a, b) Lung window images of thin-section CT scans (1.5-mm section thickness) obtained at levels of aortic arch (a) and right inferior pulmonary vein (b), respectively, show small centrilobular nodules (arrowheads), tree-in- bud signs (arrows), bronchiolectasis (open arrows), and area of mosaic attenuation (curved arrows) in both lungs. (c) Low-magnification (×40)

photomicrograph of surgical lung biopsy obtained from right lower lobe demonstrates marked membranous bronchiolar wall thickening (arrows) with lymphocytes and macrophages. (d) A more closer look (×100) of the inflamed bronchiole discloses bronchiolar wall thickening with chronic inflammatory cell infiltration and patchy aggregates of fibrosis. Surrounding alveolar walls contain many foamy macrophages (arrows)

Nontuberculous Mycobacterial

Pulmonary Disease

Pathology and Pathogenesis

Chronic progressive disease also resembles tuberculosis, with upper lobe thin-walled cavities and granulomatous inflammation, with or without caseous necrosis. This presentation most often is seen in patients with underlying chronic lung disease such as chronic obstructive pulmonary disease (COPD), bronchiectasis, cystic fibrosis, pneumoconiosis, reflux disease, or preexisting cavitary lung disease of any cause. The differentiation of tuberculosis from NTM disease could not be accurately made based solely on the histologic

features (Fig. 18.5). However, the airway-centered tendency of NTM reflects an airborne etiology, and this could be correlated with the classification according to the radiologic findings. In addition, coexisting constitutional lung diseases, and especially bronchiectasis, were suspected to be predisposing conditions for NTM organisms to colonize and progress to true NTM pulmonary disease [22].

Symptoms and Signs

NTM lung infection presents with diverse manifestations. Symptoms of bronchiectasis including cough, sputum production, and hemoptysis can occur. Tuberculosis-like